On a cellular level, the ion channels most directly associated with repolarization are potassium-conducting, and thus most medications and genes associated with QT prolongation have effects on potassium currents. Specifically, blockade of the HERG/KCNH2 (IKr) ion channel has been implicated in the majority of drug-induced QT prolongation6, although other ion currents are involved in congenital long QT syndrome, including the IKs (KCNQ1 and KCNE1), INa (SCN5A), and IK1 (KCNJ2).